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Colorectal cancer (CRC) is the third leading cause of cancer-related deaths and a major health problem. High mobility group box 3 (HMGB3), a member of the high-mobility group box (HMGB) family, was reported to be over-expressed in gastric carcinoma and bladder cancer. However, the function of HMGB3 in CRC remains unclear. Here, we found that HMGB3 was up-regulated in CRC at both mRNA and protein levels. qRT-PCR results showed that high expression of HMGB3 had positive correlation with serosal invasion, lymph metastasis, and tumor–node–metastasis (TNM) stage in CRC patient. Functional experiments showed that HMGB3 can promote CRC cells proliferation and migration in vitro. Moreover, we found HMGB3 can active WNT/β-catenin pathway to increase the expression level of c-Myc and MMP7. These results may be the reason for HMGB3 oncogene role in CRC. In summary, our data indicated that HMGB3 may serve as an oncoprotein and could be used as a potential prognostic marker in CRC.

Long non-coding RNAs (lncRNAs) are involved in kinds of human diseases, including colorectal cancer (CRC). TINCR, a 3.7 kb long non coding RNA, was associated with cell differentiation in keratinocyte and gastric cancer cells. However, little is known about the role of TINCR in regulation CRC progression. Here, we showed that lncRNA TINCR was associated with CRC proliferation and metastasis. TINCR was statistically downregulated in CRC tissues and metastatic CRC cell lines compared with their counterparts. TINCR was reversely correlated with CRC progression and promoted tumor cells growth, metastasis in vivo and in vitro. While overexpression of TINCR had opposite effect. In addition, we also found that TINCR specifically bound to EpCAM through RNA IP and RNA pull down assays. Loss of TINCR promoted hydrolysis of EpCAM and then released EpICD, subsequently, activated the Wnt/β-catenin pathway. Further studies shown that c-Myc repressed the expression of TINCR through repressing sp1 transcriptive activity, which established a positive feedback loop controlling c-Myc and TINCR expression. These findings elucidate that loss of TINCR expression promotes proliferation and metastasis in CRC and it could be considered as a potential cancer suppressor gene.

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BackgroundGrowing evidence suggests that MiRNAs play essential roles in the initiation and progression of colorectal cancer (CRC). The aberrant expression of miR-384 has been reported in some cancers. However, the role and mechanism of miR-384 in CRC proliferation remains unknown.MethodsThe expression of miR-384 was detected in CRC and their paired normal tissues by real-time PCR. In vivo and in vitro assays were conducted to confirm the role of miR-384 in the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro assays were used to confirm that AKT3 was the target gene of miR-384. Finally, Spearman’s correlation analyses was carried out to analyze the relationship between miR-384 expression and AKT3 expression in CRC.ResultsMiR-384 was down‑regulated in CRC tissues. The in vivo and vitro functional assays verified that the ectopic upregulation of miR-384 inhibited the proliferation of CRC and the inhibition of miR-384 promoted the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro functional assays confirmed AKT3 as the target gene of miR-384. The expression of miR-384 was negatively correlated with the expressions of AKT3.ConclusionOur study verified that miR-384 could significantly suppress the proliferation of CRC by directing targeting AKT3.Electronic supplementary materialThe online version of this article (10.1186/s12935-018-0628-6) contains supplementary material, which is available to authorized users.

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Background: The incidence and mortality of colorectal cancer (CRC) are rising worldwide. Long-noncoding RNAs (lncRNAs) are known to play key roles in the development of human cancers, including CRC. However, the function and underlying mechanism of long intergenic noncoding RNA 00707 (LINC00707) in the development of CRC are unknown. Materials and methods: The expression of LINC00707 and miR-206 in tissue samples or cell lines was measured by quantitative reverse transcription PCR (qRT-PCR). The protein expression of neurogenic locus notch homolog protein 3 (NOTCH3) and transmembrane 4 L6 family member 1 (TM4SF1) was assessed by Western blotting. Cell proliferation, migration, and invasion were assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and transwell assays. Luciferase reporter assay and biotin-coupled miRNA capture assay were used to explore the relationship between LINC00707 and miR-206 expression. Results: The expression of LINC00707 was significantly upregulated in CRC tissues as compared with the adjacent non-CRC tissues. LINC00707 expression was significantly correlated with tumor size, lymphatic metastasis, and distant metastasis, but not significantly correlated with age and gender. Knockdown of LINC00707 expression significantly inhibited LoVo and HCT116 cell proliferation, migration, and invasion. LINC00707 acted as a molecular sponge by competing for miR-206 and indirectly modulating the expression of its targets, NOTCH3 and TM4SF1. Conclusion: LINC00707 promotes CRC cell proliferation and metastasis by sponging miR-206, suggestive of its potential application for CRC treatment.